This persists through the thermal biochemical reaction phase and the biochemical inflammatory reaction phase on the time order. 

At 1–2 h postburn, there is a significant increase in capillary permeability occurring in the injured, though still viable tissues, contiguous with the necrosis caused by direct thermal injury. 

This results in exudation of intravascular fluid toward the wound surface and interstitial space while tissue ischemia is occurring. 

Simultaneously, the injured but viable tissues and cells in the area of lesion develop edema due to metabolic disorder. 

At this time, the permeable capillaries release plenty of chemical substances which not only locally aggravate the injury itself and damage the peripheral uninjured areas, but also may subsequently result in systemic injury.

Although it is not quite clear what these chemical substances are, they appear to include histamine, 5-HT, hydrogen ion, kinin and bradykinin, etc. This phase is called the ‘thermal biochemical reaction phase’. 

About 2 h later, the thermal biochemical reaction continues to affect the viable tissues in the injured area to cause a series of inflammatory reactions.

The initiation of such an inflammatory pathological reaction in the injured area may result in the full spectrum of pathological injuries. 

For instance, inflammatory reaction activates the blood coagulation system to induce progressive thrombosis of the microcirculation, which may cause necrosis of the injured but viable tissues and may also result in ischemic and anoxic necrosis of the surrounding uninjured tissues. 

This process may last for 72 h postburn and is called the ‘biochemical inflammatory reaction phase’.